The Biology of Cancer Second Edition Test Bank

The Biology of Cancer Second Edition By Robert A. Weinberg , Robert A Weinberg

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 1 The Biology and Genetics of Cells and Organisms Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 1.1

In a hypothetical cross between two fruit flies, one with red eyes and one with white eyes, all resulting progeny had red eyes. This would suggest that (Level 2) A. The red-eyed trait is recessive to white eyes.

B. The red-eyed trait is dominant to white eyes.

C. The red-eyed and white-eyed genes are co-dominant.

D. The eye color trait is most likely coded for by multiple genes.

E. None of the above.

1.2

Which of the following mutations would be MOST likely to be retained in a species gene pool? (Level 3) A. A mutation resulting in a deleterious change in a cytoskeletal protein structure B. A mutation in an exon of a gene coding for DNA repair C. A mutation in an intron of a gene coding for DNA repair D. Both A and B E. None of the above

1.3

Many cancer cells exhibit aneuploidy, meaning that they (Level 1) A. Proliferate at higher rates than normal cells.

B. Exhibit higher rates of apoptosis than normal cells.

C. Have an abnormal number of chromosomes.

D. Have a normal number of autosomes.

E. Have mutations in genes involved in the cell cycle.

1.4

Which of the following is NOT true of somatic mutations? (Level 2) A. They occur in non-germ-line cells.

B. They can be passed on to lineal descendants of the cell that was mutated.

C. They may occur at any time during an individual’s lifetime.

D. They can be passed on from parent to child.

E. They often play a role in cancer formation.

1.5

Which of the following is NOT a type of post-translational modification? (Level 2) A. A change in the base sequences of DNA B. Cleavage of a protein product by proteases C. Addition of lipid groups to the protein chain D. Glycosylation E. Methylation

1.6

The template on which ribosomes assemble the amino acids that form proteins is known as (Level 1) A. hnRNA B. messenger RNA C. ribosomal RNA D. DNA

E. None of the above

1.7

The expression of a given gene may be influenced by (Level 2) A. Activating transcription factors B. Enhancer sequences C. Histone modifications D. Changes in chromatin structure E. All of the above

1.8

Which of the following types of changes would most likely NOT be associated with increased cancer risk? (Level 3) A. A mutation resulting in higher levels of K-Ras expression B. Reduced expression of HOTAIR lncRNA C. Loss of function of the Dicer enzyme D. A mutation in K-Ras that prevents recognition by Let-7 E. None of the above

1.9

Which of the following is true of orthologous genes? (Level 1) A. They are genes in different species that evolved from a common ancestor.

B. They code for proteins having different functions.

C. They are genes located on the same chromosome.

D. They are related genes within the same species.

E. All of the above.

1.10

The discovery of which of the following enzymes allowed researchers to synthesize complementary DNA from mRNA in vitro? (Level 1)

A. DNA ligase B. DNA polymerase C. DNA synthetase D. Reverse transcriptase E. None of the above

1.11

Which of the following can contribute to the initiation of cancer? (Level 2) A. Somatic mutations B. Germ-line mutations C. Gene amplification D. Aneuploidy E. All of the above

1.12

Which of the following would be LEAST likely to contribute to transformation of a cell? (Level 2) A. A mutation resulting in a change in splicing B. A mutation in a transcription factor C. A silent mutation in an intron D. An activating mutation in an exon of a gene coding for a protein that promotes cellular proliferation E. Changes in the expression level of a miRNA that is involved in protein synthesis

Answers 1.1

B

1.2

C

1.3

C

1.4

D

1.5

A

1.6

B

1.7

E

1.8

B

1.9

A

1.10

D

1.11

E

1.12

C

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 2 The Nature of Cancer Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 2.1

Which of the following is true of carcinomas? (Level 2) A. They are responsible for >80% of Western world cancer deaths.

B. They involve cell types arising from all three embryonic germ layers.

C. They often involve epithelial cells.

D. Examples of tissue sites where they are found include the lung and pancreas.

E. All of the above.

2.2

Tumors that arise from mesenchymal cell types are called (Level 1) A. Carcinomas B. Lymphomas C. Sarcomas D. Adenocarcinomas E. Leukemias

2.3

Which of the following types of cellular changes would be considered to be malignant? (Level 2) A. Dysplasia B. Squamous cell carcinoma C. Papilloma D. Fibroma E. Adenoma

2.4

Which of the following schematics MOST likely describes the correct order of cellular changes that occur in the progression of malignancy? (Level 2) A. Normal → hyperplastic → dysplastic → neoplastic → metastatic B. Normal → dysplastic → hyperplastic → neoplastic → metastatic C. Normal → hyperplastic → dysplastic → metastatic → neoplastic D. Normal → neoplastic → dysplastic → hyperplastic → metastatic E. None of the above

2.5

Analysis of a patient’s lung tumor reveals that all of the malignant cells in this tumor have a specific chromosomal abnormality involving a fusion event between two sets of chromosomes. This MOST likely suggests that (Level 3) A. This mutation was inherited.

B. The tumor is polyclonal.

C. The tumor is monoclonal in origin.

D. A large number of normal cells simultaneously underwent this mutation.

E. None of the above.

2.6

In the revised Ames test, Bruce Ames mixed chemicals with homogenized rat liver prior to adding them to bacteria to assess their mutagenicity. What was the purpose of this step of the experiment? (Level 3) A. To determine whether the chemicals killed mammalian cells B. To determine whether the chemicals induced cancer in mammalian cells C. To detoxify the chemicals prior to assessing their mutagenicity D. To metabolically activate the chemicals prior to assessing their mutagenicity E. None of the above

2.7

Which of the following is NOT a test for mutagenicity? (Level 2) A. Proliferation assay B. Ames test C. Test for sister chromatid exchange (SCE) D. Karyotype analysis E. Analysis of micronuclei

2.8

A tumor promoter (Level 3) A. Induces mutations in DNA. B. Can cause cancer on its own.

C. Enhances tumorigenesis through nongenetic mechanisms.

D. Is always a naturally occurring compound.

E. B and C.

2.9

The level of mutagenicity of a particular chemical may depend upon (Level 2) A. Its metabolic conversion within an organism.

B. The cell type with which it comes in contact.

C. Expression levels of genes coding for proteins that are able to inactivate mutagens within the cell.

D. The presence of other tumor-promoting compounds.

E. All of the above.

2.10

Which of the following compounds was identified as being carcinogenic by the Ames test? (Level 1) A. Black pepper B. Rhubarb C. Celery D. Coffee E. All of the above

2.11

Malignant tumors (Level 2) A. Always contain a single cell type.

B. Have acquired characteristics of invasiveness.

C. Are surrounded by an intact basement membrane.

D. Are often described as being in-situ.

E. C and D.

2.12

Which of the following is true of energy metabolism by cancer cells? (Level 2) A. They usually generate ATP through the Krebs cycle.

B. They are more efficient at energy metabolism than normal cells and generate 36 molecules of ATP for every glucose molecule metabolized.

C. They generate energy through glycolysis only when cells are experiencing hypoxia.

D. They import much higher levels of glucose in comparison with normal cells.

E. None of the above.

Answers 2.1

E

2.2

C

2.3

B

2.4

A

2.5

C

2.6

D

2.7

A

2.8

C

2.9

E

2.10

E

2.11

B

2.12

D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 3 Tumor Viruses Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 3.1

Dulbecco and Rubin discovered that they could infect chicken embryo fibroblasts with RSV in culture. Which of the following was NOT a characteristic exhibited by these cells after they were infected? (Level 2) A. Virus particles were produced by these cells for many weeks.

B. Cells formed clusters, or foci, after infection.

C. The cells seemed to demonstrate uninhibited proliferation.

D. The cells exhibited flattened morphology.

E. The cells exhibited metabolic properties similar to those observed in tumor cells.

3.2

Experiments using temperature-sensitive mutants of RSV to infect chicken embryo fibroblasts demonstrated that (Level 2) A. Infection with RSV is necessary to initiate transformation of these cells, but the RSV genome is not needed to maintain the transformed state.

B. The RSV transforming gene is necessary for both the initiation and maintenance of transformation in these cells.

C. Infection with RSV alone is unable to transform these cells.

D. Cells infected with RSV continue to exhibit normal cellular morphology.

E. None of the above.

3.3

Which of the following is considered to be a tumor virus? (Level 1) A. Hepatitis B virus (HBV) B. Human papillomavirus (HPV) C. Shope fibroma virus D. Human adenovirus 5 E. All of the above

3.4

Which of the following is a property of transformed cells? (Level 2) A. Rounded shape B. Reduced requirement for mitogenic growth factors C. Loss of contact inhibition D. Increased transport of glucose E. All of the above

3.5

The ability of cells suspended in soft (semi-solid) agar medium to form colonies is a good predictor that (Level 3) A. These cells will form tumors if injected subcutaneously into immunocompromised mice.

B. These cells have stopped proliferating and will die.

C. These cells would fail to grow in normal medium.

D. These cells have an increased requirement for growth factors.

E. None of the above.

3.6

Once a cell has been infected with a virus, how might viral genes be transmitted from mother to daughter cells? (Level 2) A. Viral DNA carries its own replication machinery, replicating its own genome independently of host enzymes.

B. Viral DNA may be integrated into the host cell’s chromosomes, so that it is replicated along with host DNA prior to cell division.

C. Viral DNA may be linked to host DNA through protein bridges, allowing it to tag along with host chromosomal DNA during cell division.

D. B and C. E. All of the above.

3.7

Which of the following enzymes are encoded by retroviral DNA? (Level 2) A. Integrase.

B. Reverse transcriptase.

C. RNA polymerase II. D. A and B. E. None of these enzymes are encoded by retroviral DNA.

3.8

A gene found in a normal cell’s genome that can be picked up and altered by a virus to drive cellular transformation is known as (Level 1) A. An oncogene B. A proto-oncogene C. A transgene D. A protogene E. None of the above

3.9

Scientists may map the insertion sites of viruses in DNA isolated from tumors that formed following retroviral infection in order to (Level 3) A. Identify the viral genes responsible for transformation.

B. Discover new proto-oncogenes.

C. Determine how viruses suppress tumorigenesis.

D. Understand how viruses infect cells.

E. All of the above.

3.10

Some retroviruses are able to transform cells through (Level 2) A. Inserting themselves near a proto-oncogene in the host genome.

B. Acquiring oncogenes within their own genome.

C. Possessing genes that specify proteins that activate cellular genes involved in proliferation.

D. A, B, and C.

E. None of the above.

3.11

3.12

Which of the following is true of retroviruses? (Level 2) A.

They are DNA viruses.

B.

Their replication cycle requires DNA to be transcribed to RNA.

C.

The DNA versions of their viral genomes are called proviruses.

D.

B and C.

E.

None of the above.

Which of the following is true of c-src? (Level 2) A. It is present only in vertebrate cells containing integrated viral DNA. B. It results in cellular transformation.

C. It is an example of a proto-oncogene.

D. It is highly conserved among vertebrate species.

E. C and D.

Answers 3.1

D

3.2

B

3.3

E

3.4

E

3.5

A

3.6

D

3.7

A

3.8

B

3.9

B

3.10

D

3.11

D

3.12

E

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 4 Cellular Oncogenes Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 4.1

DNA from human lung tumor cells was used to transfect NIH 3T3 (mouse embryo fibroblast) cells. After several weeks, some of these cells formed foci, or clusters of cells, on the plate. Cells isolated from these foci were able to grow in soft agar and formed tumors when injected subcutaneously into immunocompromised mice. These results suggest that (Level 3) A. The oncogene present in the human lung tumor cells is also able to transform NIH 3T3 mouse cells.

B. The NIH 3T3 cells were most likely transformed by multiple oncogenes present in the donor cells.

C. The NIH 3T3 cells were most likely transformed by a single oncogene present in the donor cells.

D. A and C. E. A, B, and C.

4.2

Which of the following types of genetic alterations would be associated with an increased aggressiveness of cancer cells? (Level 2) A. Amplification of ErbB2

B. Amplification of Myc C. Decreased expression of ErbB2 D. Lower expression of Myc E. A and B

4.3

Which of the following statements is TRUE? (Level 2) A. All types of cancer are associated with a transforming retrovirus.

B. Breast cancer patients whose tumors express elevated levels of ErbB2 usually have a longer median survival after diagnosis than those with normal levels of this protein.

C. Retrovirus-associated oncogenes are often related to the oncogenes found in increased copy numbers in non-virally induced tumor cells.

D. Patients with bladder cancer often have reduced levels of H-Ras expression.

E. None of the above.

4.4

Oncogenic mutations in H-Ras are most often the result of (Level 2) A. Point mutations resulting in a premature stop codon.

B. Point mutations that change the protein’s structure and result in its constitutive activation.

C. Insertion of extra bases in exon 1 of the gene.

D. Frameshift mutations.

E. None of the above.

4.5

Which of the following mechanisms may contribute to tumorigenesis driven by the myc oncogene? (Level 2) A. Increased myc copy number B. Constitutive activation of myc under the transcriptional control of viral promoters C. Chromosomal translocations D. A, B, and C E. None of the above

4.6

Fusion of the reading frames of the bcr and abl genes, as is often observed in cases of chronic myelogenous leukemia (CML), is an example of what type of genetic alteration? (Level 1) A. A reciprocal chromosomal translocation B. A nonreciprocal chromosomal translocation C. A frameshift mutation D. A chromosomal deletion E. None of the above

4.7

The transforming abilities of the Bcr-Abl fusion protein are due primarily to the deregulated firing of its tyrosine kinase, which is equivalent to what domain of the normal Abl protein? (Level 2) A. The SH1 domain B. The SH2 domain

C. The SH3 domain D. The DNA binding domain E. None of the above

4.8

Approximately what percentage of human tumors are associated with infectious agents? (Level 1) A. 5% B. 10% C. 20% D. 40% E. 60%

4.9

Which of the following factors are associated with Burkitt’s lymphoma formation?

(Level 2) A. Malarial infection B. Infection with Epstein–Barr virus (EBV) C. Mutation in c-myc D. Mutation in ErbB2 E. A, B, and C

4.10

Which of the following consequences of mutations would be LEAST likely to be associated with an increased cancer risk? (Level 3) A. Truncation of the EGF receptor

B. Amplification of myc C. Amplification of ErbB2 D. Truncation of H-Ras due to a premature stop codon.

E. Constitutive activation of K-Ras

4.11

Normal proto-oncogenes found in the human genome can be activated to become oncogenes by (Level 2) A. Somatic mutations that result in higher levels of expression of the gene.

B. Deregulation by retroviral elements.

C. Mutations resulting in structural changes in the protein product of the gene.

D. A, B, and C. E. None of the above.

4.12

Gene amplification can be detected by A. Observation of homogeneously staining regions using microscopy.

B. Deletion of the arm of a chromosome.

C. Observation of extrachromosomal “double minutes.”

D. A and C. E. None of the above.

Answers 4.1

D

4.2

E

4.3

C

4.4

B

4.5

D

4.6

A

4.7

A

4.8

C

4.9

E

4.10

D

4.11

D

4.12

D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 5 Growth factors, Receptors, and Cancer Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 5.1

You are growing NIH 3T3 (mouse embryonic fibroblasts) in a Petri dish. You provide these cells with a medium containing amino acids, glucose, vitamins, and salts necessary for their survival, but you run out of serum to supplement the medium. Without the addition of serum, what will MOST likely happen to these cells? (Level 3)

5.2

A.

The cells will die.

B.

The cells will continue to grow and proliferate as usual.

C.

The cells will remain viable, but will not grow and divide.

D.

The cells will proliferate at a higher than normal rate.

E.

None of the above.

Which of the following is NOT true of the Src protein? (Level 2) A.

Src operates as a protein kinase.

B.

Src phosphorylates ADP to make ATP.

C.

Src can serve as a kinase substrate.

D.

A and C.

E.

5.3

None of the above.

Mutations in the EGF receptor (EGF-R) that contribute to the development of cancer are MOST often due to (Level 2) A. Truncation of the ectodomain of the receptor.

B. Elongation of the ectodomain of the receptor.

C. Point mutations in the C-terminus of the receptor.

D. Point mutations in the tyrosine kinase domain of the receptor.

E. C and D.

5.4

Which of the following is NOT an example of a tyrosine kinase growth factor receptor that is often altered in cancer cells? (Level 1) A. ErbB2 B. Kit C. FGF-R2 D. VEGF E. PDGF-Rβ

5.5

In cells infected with simian sarcoma virus, the sis oncogene causes the cells to release increased amounts of Sis protein, which is recognized by PDGF-receptor molecules on the cells’ surface. This type of signaling loop is an example of (Level 2) A. Endocrine signaling.

B. Paracrine signaling.

C. Autocrine signaling.

D. Trans-receptor signaling.

E. None of the above.

5.6

When a growth factor receptor is not bound to ligand, it is MOST likely in what configuration? (Level 2) A. Monomeric B. Dimeric C. Trimeric D. Heterodimeric E. None of the above

5.7

Which of the following statements about TGF-β receptors is FALSE? (Level 2) A. They have an extracellular ligand-binding and a transmembrane domain.

B. Their kinase domains phosphorylate serine and threonine residues.

C. Type I and Type II TGF-β receptors form heterodimers.

D. A and C. E. None of the above.

5.8

Which of the following statements is TRUE of the ligands of nuclear receptors?

(Level 2)

A. They are hydrophobic.

B. They may activate transcription factors.

C. They include steroid sex hormones, retinoids, and vitamin D. D. A, B, and C. E. None of the above.

5.9

Cell surface receptors that are able to create mechanical stability by tethering cells to the extracellular matrix (ECM) are known as (Level 1)

5.10

A.

Adhesions.

B.

Matrix metalloproteinases.

C.

Integrases.

D.

Integrins.

E.

Cytokines.

Which of the following statements is FALSE regarding Ras mutations in cancer patients? (Level 3) A.

Mutations often occur at codons 12, 13, or 61.

B.

Oncogenic mutations usually result in higher levels of GDP-bound Ras.

C.

Oncogenic mutations usually result in higher levels of GTP-bound Ras.

D.

Cells often have compromised activity of GTPase-activating proteins (GAPs).

E.

None of the above.

5.11

5.12

Overexpression of growth receptors helps to promote cancer growth by (Level 2) A.

Stimulating the dimerization and transphosphorylation of the receptors.

B.

Turning off downstream signaling.

C.

Promoting mitogenic signaling.

D.

A and C.

E.

None of the above.

Ligand-independent signaling of receptor-tyrosine kinases can result from A.

Fusion events that prevent dimerization.

B.

Mutations resulting in truncation of the receptor ectodomain.

C.

Amino acid substitutions in the cytoplasmic domains of receptors.

D.

B and C.

E.

None of the above.

Answers 5.1

C

5.2

B

5.3

A

5.4

D

5.5

C

5.6

A

5.7

E

5.8

D

5.9

D

5.10

B

5.11

D

5.12

D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 6: Cytoplasmic Signaling Circuitry Programs Many of the Traits of Cancer Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 6.1

Following serum starvation, if normal fibroblasts were treated with cycloheximide to shut down cellular protein synthesis, then, when exposed to fresh serum, the cells would (Level 2) A. Continue to remain viable in a quiescent state.

B. Express immediate early genes.

C. Enter a state of senescence.

D. Die. E. None of the above.

6.2

What happens in cells following stimulation with growth factors? (Level 2) A. The transcription of all genes required for growth and replication occurs immediately.

B. There is a delay of several hours before transcription of genes needed for growth occurs.

C. Some genes required for growth are transcribed immediately, while others are transcribed later, after new transcription factors have been synthesized.

D. Cell death occurs.

E. None of the above.

6.3

Which of the following is NOT true of the son of sevenless (Sos) protein? (Level 2) A. It is a guanine nucleotide exchange factor (GEF).

B. It is a GTPase-activating protein (GAP).

C. It is able to activate Ras. D. It was initially identified in Drosophila melanogaster.

E. None of the above.

6.4

Which of the following domains of Src is its catalytic domain? (Level 1) A. SH1 B. SH2 C. SH3 D. C-terminus E. N- terminus

6.5

The SH2 domains of tyrosine kinases function to (Level 3)

A. Catalyze activation of downstream pathways.

B. Act as receptors for phosphotyrosine-containing oligopeptide ligands.

C. Localize the protein to specific sites in the cell.

D. B and C. E. None of the above.

6.6

Which of the following signaling pathways is in the correct order? (Level 2) A. Receptor → Sos → Grb2 → Ras B. Receptor → Ras → Sos → Grb2 C. Receptor → Sos → Ras → Grb2 D. Receptor → Grb2 → Ras → Sos E. Receptor → Grb2 → Sos → Ras

6.7

Which of the following molecules is NOT a downstream effector of Ras? (Level 2) A. Ral-GEFs B. PI3K C. Grb2 D. Raf E. None of the above

6.8

Which of the following statements about AKT is FALSE? (Level 3)

A. AKT is activated downstream of PI3K. B. AKT activation may inhibit apoptosis through downstream inactivation of Bad. C. AKT activation may result in activation of mTOR. D. AKT is tethered to the plasma membrane by PIP3.

E. None of the above.

6.9

Which of the following pathways activated downstream of Ras can result in reorganization of the cytoskeleton, playing a role in cell motility? (Level 2) A. MEK B. PI3K C. Ral BP1 D. Erk1 E. None of the above

6.10

Which of the following is NOT true of β-catenin? (Level 2) A. It binds directly to the Wnt protein.

B. It associates with Tcf/Lef transcription factors in the nucleus, driving cell proliferation.

C. It can be degraded when bound to active GSK-3β.

D. It exists in a soluble pool in the cytosol.

E. None of the above.

6.11

In normal cells, Ras-GAPs trigger GTPase activity in order to (Level 2) A. Maintain Ras in its active state.

B. Enhance downstream signaling by Ras effectors.

C. Promote cellular proliferation.

D. Inactivate Ras signaling.

E. A and B.

6.12

Which of the following does NOT occur downstream of epidermal growth factor binding to its receptor? (Level 3) A. NF1 is phosphorylated.

B. NF1 levels are increased.

C. Ras is GTP-loaded.

D. The MAPK pathway is activated.

E. None of the above.

Answers 6.1.

B

6.2.

C

6.3.

B

6.4.

A

6.5.

D

6.6.

E

6.7.

C

6.8.

E

6.9.

C

6.10. A 6.11. D 6.12. B

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 7 Tumor Suppressor Genes Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 7.1

When a normal cell and a cancer cell were fused, the resulting hybrids lost the ability to form tumors in mice. This suggests that (Level 3) A. The cancer cell alleles are dominant over the normal cell alleles.

B. The cancer cell alleles are recessive to the normal cell alleles.

C. The normal and cancer cell alleles are co-dominant.

D. The original tumor formed as a result of infection by a tumor virus.

E. None of the above.

7.2

Sporadic cases of retinoblastoma require (Level 3) A. One inactivating somatic mutation in one copy of Rb. B. Two somatic inactivating mutations, one in each of the two copies of Rb. C. One somatic mutation in Rb, leading to its activation.

D. Two somatic mutations in a copy of Rb, leading to its activation.

E. None of the above.

7.3

Loss of heterozygosity (LOH) at a given locus may occur as the result of (Level 2)

A. Mitotic recombination.

B. Gene conversion.

C. Loss of a chromosomal region.

D. Nondisjunction.

E. All of the above.

7.4

Single nucleotide polymorphism markers (SNPs) are found approximately how far apart across the genome? (Level 1) A. Every 1 megabase B. Every 10 megabases C. Every 1 kilobase D. Every 10 kilobases E. None of the above

7.5

Which of the following is TRUE of methylation in cancer cells? (Level 2) A. Overall levels of methylation throughout the cancer cell genome often increase.

B. There is an increase in DNA methyltransferase enzyme activity.

C. Areas of CpG islands are hypomethylated.

D. Areas of CpG islands become methylated inappropriately.

E. None of the above.

7.6

The APC protein (Level 2) A. Is essential for degrading β-catenin.

B. Causes increased activation of β-catenin.

C. Helps to regulate cell motility.

D. A and C. E. None of the above.

7.7

Which of the following statements about NF1 is FALSE? (Level 2) A. It regulates Ras signaling through positive feedback control mechanisms.

B. Cells lacking NF1 have higher levels of GTP-bound Ras. C. NF1 is known as a Ras-GAP. D. B and C. E. None of the above.

7.8

You are studying a cell line in which the loss of just one copy of a tumor suppressor gene provides a growth advantage for the cells. This would be an example of genetic (Level 1) A. Haplosufficiency.

B. Heteroinsufficiency.

C. Haploinsufficiency.

D. Unilateral mutation.

E. None of the above.

7.9

HIF-1α levels may go up when (Level 3) A. Oxygen conditions are at normal physiologic levels.

B. Cells are experiencing hypoxic conditions.

C. Oxygen levels are high.

D. HIF-1α is bound to pVHL.

E. C and D.

7.10

Which of the following genes is NOT classified as a tumor suppressor? (Level 2) A. MGMT B. p16INK4A C. PTEN D. VHL E. None of the above

7.11

Inactivation of tumor suppressor genes can occur as the result of (Level 2) A. Somatic mutation.

B. Promoter demethylation.

C. Loss of heterozygosity.

D. A and C. E. None of the above.

7.12

You are studying cancer cells, and hypothesize that you have found a previously unidentified tumor suppressor gene. Which of the following results would support your hypothesis? (Level 3) A. You have found loss of heterozygosity in the locus containing your gene in a number of human lung cancer samples.

B. You have identified a gain-of-function mutation in this gene that results in the transformation of normal cells.

C. Functional analysis has revealed that the wild-type form of the gene that you have identified serves to drive proliferation.

D. B and C.

E. None of the above.

Answers 7.1

B

7.2

B

7.3

E

7.4

C

7.5

D

7.6

D

7.7

A

7.8

C

7.9

B

7.10

A

7.11

D

7.12

A

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 8 pRb and Control of the Cell Cycle Clock Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge

8.1

The resting, nonproliferative phase of the cell cycle is (Level 1) A. G0.

B. G1.

C. G2.

D. S. E. M.

8.2

The critical decision point at which a cell determines its fate at the end of the G1 phase of the cell cycle is called (Level 1) A. The transition point.

B. The resolution point.

C. The commitment point.

D. The restriction point.

E. The contraction point.

8.3

Which of the following statements is NOT true of the pRb protein? (Level 3) A. pRb is functionally inactive when it is hyperphosphorylated.

B. pRb is mostly unphosphorylated during the G0 phase of the cell cycle.

C. pRb is growth-promoting during early G1 phase.

D. pRb phosphorylation is initiated by D-type cyclins and CDK4/6.

E. pRb is functionally inactivated at the R point.

8.4

Which of the following types of mutations would NOT be advantageous to a cancer cell? (Level 2) A. An inactivating mutation in pRb B. An inactivating mutation in a gene controlling a DNA damage checkpoint C. An inactivating mutation in p16INK4A D. An inactivating mutation in cyclin D E. An inactivating mutation in p19INK4D

8.5

The cyclin/cyclin-dependent kinase pair that is active during the M phase of the cell cycle is (Level 2) A. Cyclin A/CDC2.

B. Cyclin B/CDC2.

C. Cyclin D/CDK4/6.

D. Cyclin E/CDK2.

E. Cyclin A/CDK2.

8.6

An increase in cyclin D activity may result from all of the following EXCEPT (Level 3) A. Activation of the Ras signaling pathway.

B. Activation of the Hedgehog signaling pathway.

C. An increase in NF-κB expression.

D. A decrease in STAT expression.

E. A decrease in p16INK4A expression.

8.7

Levels of cyclin A are highest during the phase of the cell cycle in which (Level 3) A. The cell prepares to enter a quiescent state.

B. Mitosis occurs.

C. The cell is most responsive to mitogenic growth factors.

D. Cytokinesis occurs.

E. DNA replication occurs.

8.8

Cyclin D/CDK4/6 complexes can be inhibited by (Level 2) A. p27Kip1.

B. p15INK4B. C. p57Kip2.

D. p21Cip1.

E. AP-1.

8.9

All of the following are true of the R point EXCEPT (Level 2) A. It occurs at the G2/M transition.

B. The cell’s fate at this point may be influenced by growth factors in the cell’s surroundings.

C. Deregulation of signaling controlling the R point is common in cancer cells.

D. It is followed by the activation of cyclin E/CDK2 complexes.

E. Passage through this point is regulated by phosphorylation of pRb.

8.10

When a cell is at G0, pRb is (Level 2) A. Undetectable.

B. Unphosphorylated.

C. Hypophosphorylated.

D. Hyperphosphorylated.

E. Overexpressed.

8.11

Histone deacetylase (HDAC) enzymes (Level 2) A. Promote initiation of transcription.

B. Complex with hyperphosphorylated pRb. C. Repress E2F family activity.

D. Add acetyl groups to E2F promoters.

E. Promote initiation of translation.

8.12

Which of the following scenarios may contribute to the hyperphosphorylation of pRb? (Level 3) A. Inactivation of the Ras pathway B. Inactivation of p21Cip1 C. Activation of p15INK4B D. Inactivation of NF-κB E. Activation of Smad3/4

8.13

Activation of Myc may result in all of the following EXCEPT (Level 3) A. Hyperphosphorylation of pRb. B. Increased expression of CDK4.

C. Degradation of p27Kip1.

D. Increased transcription of target genes by E2F transcription factors.

E. Decreased activation of cyclin E/CDK2 complexes.

8.14

Which of the following may result from activation of TGF-β? (Level 3) A. Increased activation of cyclin D/CDK4/6 complexes B. Increased expression of p21Cip1 in the cytoplasm of the cell C. Reduced expression of p15INK4B D. Decreased activation of cyclin E/CDK2 complexes

E. Phosphorylation of Smad4

8.15

pRb in cells undergoing differentiation will generally be (Level 2) A. Unphosphorylated.

B. Hyperphosphorylated.

C. Bound to E2F transcription factors.

D. Inactivated.

E. Bound to histone acetylases.

8.16

Which of the following types of mutations are MOST likely to be found in cancer cells?

A. Activating mutations in pRb B. Mutations resulting in deregulation of the restriction point C. Mutations resulting in enhanced restriction point regulation D. Mutations that promote differentiation E. C and D

8.17

In a normal cell, signals from the external environment play a role in determining whether the cell will grow or replicate during what phase(s) of the cell cycle?

A. The S phase only B. The G1 phase only C. The G2 phase only

D. Both the G2 and S phases E. All phases of the cell cycle

Answers 8.1

A

8.2

D

8.3

C

8.4

D

8.5

B

8.6

D

8.7

E

8.8

B

8.9

A

8.10

B

8.11

C

8.12

B

8.13

E

8.14

D

8.15

C

8.16

B

8.17

B

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 9

p53 and Apoptosis: Master Guardian and Executioner

Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 9.1

An irreversible arrest in the cell cycle resulting in a viable but nongrowing state is known as (Level 1) A. The arrest point.

B. Senescence.

C. Quiescence.

D. Inactivation.

E. Involution.

9.2

The process of formation of new blood vessels is called (Level 1) A. Leukemogenesis.

B. Hematopoiesis.

C. Vasculogenesis.

D. Thrombopoiesis.

E. Angiogenesis.

9.3

The cell’s latent suicide program, resulting in rapid cell death, is called (Level 1) A. Apoptosis.

B. Necrosis.

C. Eradication.

D. Ischemia.

E. Caspase.

9.4

Which of the following is NOT true of p53? (Level 1) A. Most tumor-associated p53 mutations are the result of nonsense codons.

B. p53 is mutated in over 30–50% of all cancers.

C. Normal p53 functions as a “tumor suppressor.”

D. Mice lacking p53 are viable.

E. Exposure to UV radiation results in increased expression of p53.

9.5

p53 signaling may result in all of the following EXCEPT (Level 2) A. Apoptosis.

B. Senescence.

C. Angiogenesis.

D. DNA repair.

E. Cytostatic response.

9.6

Increased expression of MDM2 may result in (Level 2)

A. Increased expression of p53.

B. Apoptosis.

C. Cell cycle arrest.

D. Degradation of p53.

E. Senescence.

9.7

Which of the following types of p53 mutations would be MOST beneficial to a tumor cell? (Level 2) A. Splice site change.

B. Premature stop codon.

C. Silent mutation.

D. Frameshift.

E. Missense mutation.

9.8

DNA damage may result in all of the following EXCEPT (Level 2) A. Increased activation of ATM. B. Increased activation of Chk1/Chk2.

C. Increased levels of p53 protein.

D. DNA double strand breaks.

E. Ubiquitylation of p53.

9.9

The p14ARF protein may be activated in response to all of the following EXCEPT

(Level 2) A. Ras signaling.

B. Increased levels of E1A. C. Decreased activity of E2F transcription factors.

D. C-Myc signaling.

E. None of the above.

9.10

Which of the following types of alterations would NOT promote tumorigenesis?

(Level 3) A. Overexpression of MDM2 B. Overexpression of Bak C. Overexpression of Bcl-2 D. Defective Chk2 kinase signaling E. Increased activation of PI3K

9.11

Which of the following proteins has a BH4 domain? (Level 2) A. Bax B. Bid C. Puma D. Bcl-2 E. Hrk

9.12

Release of cytochrome c from the mitochondrial membrane is stimulated by (Level 2) A. Bcl-2 and Bcl-XL. B. Bax and Bad. C. Bcl-W and Mcl-1.

D. Caspase-9.

E. None of the above.

9.13

Which of the following scenarios will NOT result in an increase in apoptotic activity? (Level 3) A. Overexpression of Noxa B. Inhibition of Bcl-2 signaling C. Phosphorylation of Bim D. Activation of caspase-9 E. Flux in cellular calcium levels

9.14

Which of the following proteins may INHIBIT apoptosis? (Level 2) A. Bcl-2 B. Caspase-9 C. Lamin D. Apaf-1 E. Noxa

9.15

Which of the following results in an increase in the levels of p53 protein? (Level 1) A. Oncogenic signaling B. UV radiation C. Ionizing radiation D. Hypoxia E. All of the above

9.16

Apoptotic cell death can be induced by (Level 2) A. p53 signaling.

B. Signaling from surface cell death receptors.

C. Extracellular stresses.

D. A, B, and C. E. None of the above.

Answers 9.1

B

9.2

E

9.3

A

9.4

A

9.5

C

9.6

D

9.7

E

9.8

E

9.9

C

9.10

B

9.11

D

9.12

B

9.13

C

9.14

A

9.15

E

9.16

D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 10 Eternal Life: Cell Immortalization and Tumorigenesis Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 10.1

Which of the following is NOT commonly present at high levels in senescent cells? (Level 2) A. p16INK4A B. p21Cip1 C. SV40 large T antigen D. β-galactosidase enzyme E. None of the above

10.2

Which of the following is NOT a common characteristic of human senescent cells? (Level 2) A. Heterochromatic foci present in the nucleus B. Positive staining for Ki67 C. Large cytoplasm D. “Fried egg” appearance in culture E. None of the above

10.3

The structures located at the ends of chromosomes for protection and for

prevention of end-to-end fusion are known as (Level 1) A. Centromeres.

B. Telomeres.

C. Telocaps.

D. Shields.

E. Chromosome end clocks.

10.4

In normal cells, the telomeric DNA sequences (Level 1) A. Get shorter with successive cell generations.

B. Get longer with successive cell generations.

C. Remain unchanged throughout successive cell generations.

D. Disappear after the first generation of daughter cells.

E. None of the above.

10.5

Which of the following is MOST likely true of aggressively dividing cancer cells?

(Level 2) A. They do not express telomerase.

B. They do not express hTERT. C. They are in a state of cell crisis.

D. Their telomeres are stabilized (not shortening with each cellular division).

E. None of the above.

10.6

Which of the following proteins is NOT part of the shelterin complex? (Level 2) A. TRF1

B. TRF2 C. POT1 D. TIN2 E. None of the above

10.7

Human cancer cells that lack telomerase activity may (Level 3) A. Be in crisis.

B. Have shorter telomeric repeat sequences.

C. Demonstrate the exchange of sequence information between telomeres through unequal crossing over.

D. Undergo chromosomal translocations.

E. All of the above.

10.8

Why does loss of telomerase activity in humans lead to severe phenotypes in the first generation, while loss of telomerase activity in laboratory mice takes several generations to exhibit any sort of phenotype? (Level 3) A. Mouse cells have shorter telomeres.

B. Human cells have shorter telomeres.

C. Mouse cells express higher levels of hTERT. D. Human cells express higher levels of hTERT. E. The length of mouse telomeres does not change over time.

10.9

Which of the following mechanisms would NOT contribute to cancer cell transformation? (Level 3) A. Erosion of telomeric DNA

B. Regeneration of telomeric DNA through the ALT mechanism C. Repeated breakage–fusion–bridge (BFB) cycles D. Stabilization of telomeres E. Increased expression of telomerase

10.10 Breakage–fusion–bridge (BFB) cycles may help drive tumorigenesis by (Level 3) A. Shortening telomeric DNA. B. Driving cellular proliferation.

C. Promoting telomere instability.

D. Providing a means for cells to acquire additional mutations.

E. Increasing expression levels of hTERT.

10.11 Which of the following is NOT a characteristic of aging cells? (Level 2) A. Lengthening of telomeric DNA sequence B. Increased telomere erosion C. Accumulation of telomere-dysfunction–induced foci (TIFs) D. B and C E. None of the above

10.12 Some cancer cells escape crisis by A. Overexpressing hTERT. B. Activating the ALT mechanism.

C. Shortening their telomeres.

D. A and B.

E. None of the above.

10.13 Which of the following statements is TRUE? A. Senescent cells can be induced to proliferate.

B. Senescent cells are viable.

C. Senescent cells are undergoing cell death.

D. Senescence is a key step in promoting neoplastic proliferation.

E. None of the above.

Answers 10.1

C

10.2

B

10.3

B

10.4

A

10.5

D

10.6

E

10.7

E

10.8

B

10.9

A

10.10 D 10.11 A 10.12 D 10.13 B

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 11 Multi-Step Tumorigenesis Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge

11.1

Patients with colon cancer often exhibit loss of heterozygosity at specific chromosomal arms. These chromosomal regions most likely include genes that act as (Level 2) A. Pro-apoptotic genes.

B. Oncogenes.

C. Tumor suppressors.

D. Tumor promoters.

E. None of the above.

11.2

Which of the following is characteristic of field cancerization? (Level 2) A. A single tumor grows from a single mutant cell.

B. Multiple tumors in an organ are separated by normal tissue.

C. Multiple tumors in an organ share the same germ-line mutation.

D. B and C. E. A, B, and C.

11.3

Which of the following observations would support the Darwinian theory for the evolution of cancer cells? (Level 3) A. Cells of the same type isolated from a tumor are all found to have multiple identical mutations.

B. Cells of the same type isolated from a tumor are found to be genetically distinct and have different types of mutations.

C. Cells isolated from a tumor are all found to have an inactivating mutation in a gene that is normally pro-apoptotic.

D. A and C. E. None of the above.

11.4

A cell representing an intermediate between stem cells and their differentiated descendants is known as a (Level 1) A. Precursor cell.

B. Transit-amplifying/progenitor cell.

C. Self-renewing stem cell.

D. Post-mitotic cell.

E. None of the above.

11.5

The rate at which mutations occur in the cells within a tumor is most likely (Level 2) A. The same as in normal cells of that tissue type.

B. Less frequent than in normal cells of that tissue type.

C. More frequent than in normal cells of that tissue type.

D. Affected by genome instability within the tumor cells.

E. C and D.

11.6

Which of the following types of mutations would NOT be advantageous for the survival of a cancer cell? (Level 3) A. An inactivating mutation in a tumor suppressor gene B. An inactivating mutation in an oncogene C. An inactivating mutation in a gene that promotes apoptosis D. Methylation of the promoter of a tumor suppressor gene E. B and D

11.7

In experiments in which rat embryo fibroblasts were transfected with suspected oncogenes, introduction of which of the following genes transformed the cells?

(Level 2) A. Myc alone B. H-Ras alone C. E1A alone D. Both Myc and E1A together E. Both Myc and H-Ras together

11.8

Transformation of some types of human cells has been achieved through insertion of cloned genes coding for (Level 2) A. Oncogenic H-Ras alone.

B. SV40 early region and hTERT together.

C. SV40 early region and oncogenic H-Ras together.

D. hTERT and oncogenic H-Ras together.

E. Oncogenic H-Ras, SV40 early region, and hTERT together.

11.9

When experimental mice are treated with DMBA and TPA to induce the formation of papillomas, TPA (Level 2) A. Serves as the initiating agent.

B. Serves as the promoting agent.

C. Must be administered multiple times in order for papillomas to form.

D. B and C. E. None of the above.

11.10 Which of the following statements is FALSE? (Level 2) A. Inflammatory cells are often detected in tumor samples.

B. Cancer often arises at sites of chronic inflammation.

C. Use of NSAIDs has been associated with increased mortality from colorectal cancer.

D. The inflammatory cytokine TNF has been shown to have direct transforming properties.

E. Levels of macrophage infiltration in tumors have been negatively correlated with patient prognosis.

11.11 Which of the following is thought to have tumor-promoting characteristics? (Level 1) A. Helicobacter pylori B. Estrogen C. Testosterone D. Hepatitis B virus E. All of the above

11.12 The ability of cells to form a tumor is usually (Level 2) A. The result of multiple mutations.

B. Influenced by chemicals that are nonmutagenic but act as promoters.

C. A quick process.

D. A and B. E. None of the above.

11.13 Which of the following is true of “complete carcinogens”? (Level 2) A. They are capable of initiating tumorigenesis.

B. They promote tumorigenesis.

C. They can induce tumor formation in laboratory animals on their own without the application of additional chemicals.

D. A, B, and C E. None of the above.

Answers 11.1

C

11.2

B

11.3

D

11.4

B

11.5

E

11.6

B

11.7

E

11.8

E

11.9

D

11.10 C 11.11 E 11.12 D 11.13 D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 12 Maintenance of Genomic Integrity and the Development of Cancer Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 12.1

A patient with chronic myelogenous leukemia (CML) exhibits chromosomal translocations in both lymphocytes and myeloid cells. This suggests that the cell in which the initiating mutation occurred was MOST likely (Level 2) A. A lymphocyte.

B. A macrophage.

C. A neutrophil.

D. A hematopoietic stem cell.

E. A myeloid precursor.

12.2

The DNA polymerase pol-δ (Level 2) A. Is involved in DNA synthesis.

B. Is involved in proofreading newly synthesized DNA. C. Exhibits exonuclease activity.

D. A, B, and C. E. None of the above.

12.3

Which of the following may result in point mutations that can contribute to

cancer? (Level 3) A. Deamination of 5-methylcytosine B. Unrepaired single-strand breaks during DNA synthesis C. Microsatellite instability D. Exposure to UV radiation E. All of the above

12.4

Keratoses, or benign skin lesions, often exhibit (Level 2) A. Mutant p53 alleles.

B. Mutations carrying a dipyrimidine substitution.

C. Mutations resulting from exposure to UV light.

D. A, B, and C. E. None of the above.

12.5

The chemical structure formed from the reaction of a DNA base with a carcinogen is called (Level 1) A. A lesion.

B. An adduct.

C. An ultimate carcinogen.

D. A xenobiotic.

E. None of the above.

12.6

Defects in which of the following cellular processes may contribute to an increased incidence of cancer? (Level 1) A. Nucleotide-excision repair

B. Mismatch repair C. Base-excision repair D. A , B, and C E. None of the above

12.7

Which of the following is true of the BRCA1 gene? (Level 2) A. Its product normally functions in DNA repair.

B. Germ-line mutations in this gene are associated with an increased risk for breast and ovarian cancers.

C. Somatic mutations in this gene are associated with an increased risk for ovarian cancer.

D. A, B, and C. E. None of the above.

12.8

Mutations that result in compromised function of the spindle assembly checkpoint during mitosis may directly contribute to (Level 2) A. Impaired p53 function.

B. Impaired DNA replication.

C. Aneuploidy.

D. A and B. E. None of the above.

12.9

Which of the following may result in loss of function of a tumor suppressor gene?

(Level 3) A. Nondisjunction of sister chromatids

B. Failure of a chromatid containing a tumor suppressor gene to attach to a spindle fiber during cell division C. Hypermethylation of the promoter for the gene D. A, B, and C E. None of the above

12.10 Which of the following types of cells are most protected from genomic damage?

(Level 2) A. Stem cells B. Differentiated cells C. Transit-amplifying cells D. Dividing cells E. A, B, and C

12.11 Which of the following types of mutations are advantageous to cancer cell growth? (Level 2) A. Those resulting in defective mismatch repair B. Inherited defects in double-strand DNA repair C. A defect in nucleotide-excision repair D. A, B, and C E. None of the above

12.12 Which of the following mechanisms is involved in double-strand DNA repair?

(Level 2) A. Homology-dependent repair

B. Nonhomologous end joining C. Mismatch repair D. A and B E. A, B, and C

Answers 12.1

D

12.2

D

12.3

E

12.4

D

12.5

B

12.6

D

12.7

D

12.8

C

12.9

D

12.10 A 12.11 D 12.12 D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 13 Dialogue Replaces Monologue: Heterotypic Interactions and the Biology of Angiogenesis Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 13.1

Which of the following is true of Hodgkin’s lymphoma? (Level 2) A. Most cells in the tumor masses of patients with this disease are neoplastic cells.

B. The neoplastic cells within Hodgkin’s lymphoma tumors are known as Reed– Sternberg cells.

C. Many normal lymphocytes are recruited to the site of neoplastic cells within patients who have this disease.

D. B and C. E. None of the above.

13.2

Stromal cells formed within various types of cancerous tumors include (Level 1) A. Fibroblasts.

B. Lymphocytes.

C. Macrophages.

D. A, B, and C. E. None of the above.

13.3

Heterotypic signaling between different cell types in a tumor often involves the activities of (Level 2) A. Trophic factors favoring cell survival.

B. Growth-inhibitory signals.

C. Mitogenic growth factors.

D. A, B, and C E. None of the above.

13.4

Many anti-cancer drugs are often first tested on cells cultured in vitro. Which of the following statements may BEST explain why these in vitro tests do not always predict clinical response to these drugs? (Level 3) A. Cancer cells grown in vitro do not proliferate as readily as they do in vivo.

B. Cancer cells grown in vitro are always anchorage-independent.

C. The conditions of in vitro culture do not recapitulate the effects of the stromal compartment of tumors operating in vivo.

D. A and B. E. A and C.

13.5

Myofibroblasts (Level 2) A. Secrete matrix metalloproteinases (MMPs).

B. Have serine in their catalytic clefts.

C. Inhibit the process of wound healing.

D. A and B. E. A, B, and C.

13.6

VEGF is involved in (Level 2) A. Monocytic migration.

B. Hematopoiesis.

C. Capillary permeability.

D. Angiogenesis.

E. All of the above.

13.7

Epithelial cells undergoing an epithelial-to-mesenchymal transition (EMT) will (Level 2) A. Migrate away from a wound site.

B. Express vimentin.

C. Express cytokeratin.

D. Exhibit a polygonal shape.

E. None of the above.

13.8

Mice in which the TGF-β type II receptor was inactivated in stromal fibroblasts exhibited (Level 3) A. Increased incidence of carcinomas.

B. Reduced incidence of carcinomas.

C. Stromal hyperplasia.

D. A and C. E. All of the above.

13.9

Colony-stimulating factor-1 (CSF-1) (Level 2) A. Recruits lymphocytes to tumors.

B. Stimulates the differentiation of monocytes to macrophages.

C. Is involved in tumor initiation.

D. Does not play a role in the development of the tumor stromal compartment.

E. None of the above.

13.10 The distance that oxygen can diffuse through living tissue is approximately (Level 1) A. 0.002 mm.

B. 0.02 mm.

C. 0.2 mm.

D. 2 mm.

E. 20 mm.

13.11 Blood vessels within tumors are (Level 2) A. Often constructed in evenly spaced patterns to provide oxygen and nutrients throughout the tumor.

B. Often constructed in a haphazard, seemingly disorganized fashion.

C. Growth-suppressed by antagonists of the VEGF receptor.

D. B and C. E. None of the above

13.12 Which of the following is NOT an angiogenic factor? (Level 1)

A. TNF-α B. Angiopoietin C. Thrombospondin-1 D. PDGF E. Leptin

13.13 Which of the following statements is FALSE? (Level 2) A. Most carcinomas depend upon stromal cells for support.

B. Tumors growing in the ascites and pleural fluid require stromal cells for structural support.

C. Many genes activated during stromal development in tumors are also activated during the wound-healing response.

D. The growth of large tumors is dependent upon the genesis of blood vessels to supply nutrients and oxygen to the cells.

E. None of the above.

13.14 Angiogenesis inhibitors are an attractive anti-cancer agent because A. They target the rapidly dividing cancer cells.

B. They target the smallest tumors at an early stage as they are starting to form.

C. They target the normal cells rather than the ever-mutating cancer cells.

D. They have no side effects.

E. None of the above.

Answers 13.1

D

13.2

D

13.3

D

13.4

C

13.5

A

13.6

E

13.7

B

13.8

D

13.9

B

13.10 C 13.11 D 13.12 C 13.13 B 13.14 C

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 14 Moving Out: Invasion and Metastasis Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 14.1

Intravasation is the movement of cancer cells from the primary site (Level 2) A. Into blood vessels.

B. Into lymphatic vessels.

C. Into distant organs.

D. A and B. E. None of the above.

14.2

The growth of microscopic metastases into macroscopic masses is known as (Level 1) A. Invasion.

B. Colonization.

C. Intravasation.

D. Extravasation.

E. None of the above.

14.3

The ability for cancer cells to form a secondary tumor at a site distant from the primary tumor (Level 2)

A. Is acquired along with the ability to move through circulation.

B. Is possessed by the majority of cells in a tumor.

C. Is often acquired after micrometastases have been established.

D. Usually occurs prior to establishment of micrometastases.

E. None of the above.

14.4

Cells that undergo an epithelial-to-mesenchymal transition will acquire (Level 2) A. Increased invasive ability.

B. Higher resistance to apoptosis.

C. Increased motility.

D. Ability to metastasize.

E. All of the above.

14.5

Cells undergoing EMT are most frequently observed (Level 2) A. In normal tissue surrounding a tumor.

B. In the center of a tumor.

C. Near the edge of a tumor.

D. Only in circulating tumor cells.

E. None of the above.

14.6

Expression of αVβ6 integrin is often expressed in epithelial cells that are involved in (Level 2) A. Chronic inflammation.

B. Wound healing.

C. EMT.

D. A, B, and C. E. None of the above.

14.7

The EMT program is regulated in part by (Level 2) A. NF-κB signaling.

B. Wnt signaling.

C. TGF-β signaling.

D. Stromal cells.

E. All of the above.

14.8

In a mouse model of breast carcinoma in which mouse mammary carcinoma cells were injected orthotopically into the mouse mammary tissue, cells in which the transcription factor Twist was knocked down by siRNA (Level 2) A. Formed primary tumors at least as rapidly as control cells.

B. Took twice as long as control cells to form tumors.

C. Had reduced metastases to the lungs.

D. A and C. E. All of the above.

14.9

Which of the following is NOT true of matrix metalloproteinases (MMPs)? (Level 2) A. They degrade the extracellular matrix surrounding tumor cells.

B. They inhibit tumor cell invasion.

C. They can cleave collagen.

D. They can be expressed in macrophages.

E. All of the above.

14.10 Small, focal protrusions from the cell surface that degrade areas of the extracellular matrix are called (Level 1) A. Invadopodia.

B. Collagenopodia.

C. Filaments.

D. Cytoskeletal arms.

E. None of the above.

14.11 Which of the following proteins may be secreted by tumor cells to drive lymphangiogenesis? (Level 2) A. VEGF-A B. VEGF-C C. PI3K D. PDGF E. None of the above

14.12 Which of the following statements is TRUE? (Level 3) A. The circulatory layout may strongly influence the location of metastases.

B. A tumor’s tendency to metastasize to particular tissues may reflect the tumor cells’ ability to adapt to the microenvironment within those tissues.

C. Colon cancer most frequently metastasizes to the lungs.

D. A and B. E. All of the above.

14.13 Matrix metalloproteinases (level 2) A. Must be inhibited for a cell to become invasive.

B. Degrade components of the extracellular matrix.

C. Are down-regulated in most cancers.

D. A and C. E. None of the above.

14.14 The majority of metastases are the result of cancer cell invasion (Level 1) A. Through blood vessels.

B. Through lymphatic vessels.

C. Through bones.

D. Through soft tissues.

E. None of the above.

Answers 14.1

D

14.2

B

14.3

C

14.4

E

14.5

C

14.6

D

14.7

E

14.8

D

14.9

B

14.10 A 14.11 B 14.12 D 14.13 B 14.14 A

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 15 Crowd Control: Tumor Immunology and Immunotherapy Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 15.1

The antigen-binding domains of an antibody molecule are made up of the (Level 1) A. Constant domains.

B. Variable domains.

C. Hinge domains.

D. Tetramer domains.

E. None of the above.

15.2

Which of the following types of cells are antigen-presenting cells? (Level 2) A. Lymphocytes B. Dendritic cells C. Macrophages D. Red blood cells E. B and C

15.3

Which of the following is NOT true of natural killer cells? (Level 2)

A. They require prior exposure to pathogens to be able to inactivate them.

B. They are involved in the innate immune response.

C. They recognize cell surface proteins on a number of cancer cells.

D. They are able to recruit additional cells to attack the target cell.

E. They release IFN-γ.

15.4

A tumor that arose in a BALB/c mouse is transplanted into a C57BL/6 mouse but does not form a tumor in the latter. This is most likely due to differences between strains in (Level 2) A. Plasma cells.

B. Helper T cells.

C. MHC proteins.

D. Complement.

E. Macrophages.

15.5

Tumor cells were grown in a BALB/c mouse, then were collected and irradiated and injected into a second BALB/c mouse. No tumor formed in the second mouse from the irradiated cells. If non-irradiated cells from the same tumor were later injected into this second mouse, what would you expect to happen? (Level 3) A. A tumor would form at the injection site.

B. No tumor would form.

C. An even more aggressive tumor than the original would form at the injection site.

D. The mouse would have a severe autoimmune reaction.

E. None of the above.

15.6

Immunocompromised individuals have significantly increased rates of (Level 2) A. All cancers.

B. Chemical carcinogen–induced cancers.

C. Virus-induced cancers.

D. B and C. E. None of the above.

15.7

Although cancer cells often express many of the same proteins on their surfaces as normal cells, they sometimes initiate an immune response by (Level 2) A. Overexpressing normal surface proteins.

B. Expressing proteins that are inappropriate for a nonembryonic cell.

C. Expressing proteins in cell types or anatomical locations in which the proteins are not usually expressed.

D. A, B, and C. E. None of the above.

15.8

Which of the following is NOT a mechanism of immunoevasion known to be utilized by cancer cells? (Level 2) A. Destruction of receptors for immune cells.

B. Release of soluble FasL. C. Neutralization of toxins within the cell.

D. Activation of complement.

E. Up-regulation of CD47 on the cell surface.

15.9

CD47, expressed on the surface of many types of cancer cells, acts to (Level 3) A. Promote cancer cell death by macrophages.

B. Protect the cancer cell from death by the host immune system.

C. Allow normal cells to be protected from the immune system.

D. B and C. E. None of the above.

15.10 Which of the following typically occurs in HER2+ breast cancer cells in response to treatment with Herceptin? (Level 3) A. Levels of phosphorylated Akt decrease.

B. Transphosphorylation of the HER3 receptor by HER2 tyrosine kinase is reduced.

C. Phosphorylation of PRAS is reduced.

D. Cells become more sensitive to radiation and chemotherapy.

E. All of the above.

15.11 Which of the following is a mechanism by which the immune response directs the killing of cancer cells? (Level 2) A. Attachment of complement to an antibody-coated cell.

B. Macrophages and natural killer cells kill the cancer cells.

C. Cytotoxic T cells kill the cells.

D. A, B, and C. E. None of the above.

15.12 Which of the following is an immunoevasive strategy used by cancer cells for

protection from the immune response? (Level 2) A. Release of TGF-β and Fas-L B. Suppression of tumor-associated antigens C. Generation of weakly antigenic variants D. A, B, and C E. None of the above

Answers 15.1

B

15.2

E

15.3

A

15.4

C

15.5

B

15.6

C

15.7

D

15.8

D

15.9

D

15.10 E 15.11 D 15.12 D

The Biology of Cancer, 2nd Edition, Question Bank © 2014 Garland Science Chapter 16 The Rational Treatment of Cancer Level 1: Comprehension of reading, knowledge of terminology Level 2: Understanding and application of information to compare and contrast or interpretation of data Level 3: Analysis and application of information to a problem, an experiment, a secondary concept, or previous knowledge 16.1

The resistance of cancer cells to EGF-R inhibition sometimes occurs as a result of (Level 2) A. Amplification of Met. B. Down-regulation of IGF-1R. C. Inhibition of Ras signaling.

D. Amplification of Gli2.

E. All of the above.

16.2

Acute promyelocytic anemia (APL) has been treated with all-trans-retinoic acid (ATRA), which results in (Level 2) A. Killing of malignant cells by NK cells.

B. Initiation of the humoral immune response.

C. Attraction of cytokines to the tumor site.

D. The differentiation of leukemic cells into neutrophils.

E. None of the above.

16.3

Cancer cells may be more susceptible than normal cells to mitotic catastrophe in

response to chemotherapeutic drugs because (Level 3) A. They express unique receptors for those drugs on their surface.

B. They may lack key G2/M checkpoint controls.

C. They may be resistant to apoptosis.

D. B and C. E. A, B, and C.

16.4

The therapeutic index of an anti-cancer drug is reflective of (Level 2) A. The dosage at which side effects are minimal.

B. Its selectivity for killing cancer cells over normal cells.

C. The method by which the drug is delivered.

D. A and B. E. None of the above.

16.5

The continued requirement of tumor cells for the initiating genetic driver for growth and viability is known as (Level 1) A. Initiator requirement.

B. Initiator addiction.

C. Oncogene addiction.

D. Oncogene promotion.

E. None of the above.

16.6

Gleevec has been used to successfully treat patients with CML by targeting (Level 2) A. Anti-apoptotic proteins.

B. The kinase activity of the Bcr-Abl fusion protein.

C. Oncogenic H-Ras signaling.

D. The antigenic proteins on the surface of leukemia cells.

E. None of the above.

16.7

Velcade has been used to treat patients with myeloma in part because of its inhibition of (Level 2) A. Ras signaling.

B. Hedgehog signaling.

C. NF-κB signaling.

D. TGF-β signaling.

E. None of the above.

16.8

In pancreatic adenocarcinoma, the tumor cells are surrounded by dense stromal tissue, making drug delivery to the cancer cells difficult. Recent studies in mice have shown improved delivery of the drugs gemcitabine and doxorubicin to pancreatic adenocarcinoma cells when concomitantly administered with antagonists of (Level 3) A. K-Ras. B. p53.

C. The Hedgehog signaling pathway.

D. PI3K. E. None of the above.

16.9

Inhibitors of the specific V600E mutant B-Raf protein have been used to treat (Level 2)

A. Melanoma.

B. Multiple myeloma.

C. Pancreatic adenocarcinoma.

D. CML. E. None of the above.

16.10 Gene expression array technology has been used to (Level 2) A. Stratify patients with breast cancer into groups predictive of response to therapy.

B. Determine the most relevant treatment for individual patients based on their genomic “signature.”

C. Predict the likelihood of disease recurrence in individuals based on gene expression signatures.

D. A, B, and C. E. None of the above.

16.11 Therapeutic antibodies used in the treatment of cancer are targeted at proteins located (Level 2) A. On the cell surface of cancer cells.

B. On the cell surface of normal cells.

C. In the nucleus of cancer cells.

D. In the cytoplasm of cancer cells.

E. C and D.

16.12 Which of the following classes of anti-cancer agents has been most successful to date? (Level 1)

A. Low–molecular-weight compounds B. Antibodies against cancer cells C. Drugs targeted against receptor-associated tyrosine kinases D. Antibiotics E. None of the above

Answers 16.1

A

16.2

D

16.3

B

16.4

D

16.5

C

16.6

B

16.7

C

16.8

C

16.9

A

16.10 D 16.11 A 16.12 C